Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Design and Long-Term Sustainability of Mini Health Centers for Primary Healthcare in Chennai, India.

Cureus·2026
Same author

ASO Visual Abstract: Evaluation of Talimogene Laherparepvec for the Treatment of Advanced Nonmelanoma Skin Cancers.

Annals of surgical oncology·2026
Same author

Evaluation of Talimogene Laherparepvec for the Treatment of Advanced Nonmelanoma Skin Cancers.

Annals of surgical oncology·2026
Same author

Development of One Health-based community surveillance system to study zoonotic diseases: a study protocol.

Frontiers in public health·2026
Same author

Frequent high-level rifaximin resistance in <i>Escherichia coli</i> associated with long-term treatment of patients with liver cirrhosis: a prospective, controlled study.

Microbiology spectrum·2025
Same author

Post-surgical outcomes in transgender women: a prospective analysis of sexual function and health-related quality of life.

World journal of urology·2025

Related Experiment Video

Updated: Apr 15, 2026

Osmotic Avoidance in Caenorhabditis elegans: Synaptic Function of Two Genes, Orthologues of Human NRXN1 and NLGN1, as Candidates for Autism
11:20

Osmotic Avoidance in Caenorhabditis elegans: Synaptic Function of Two Genes, Orthologues of Human NRXN1 and NLGN1, as Candidates for Autism

Published on: December 11, 2009

12.3K

NOMA-GAP/ARHGAP33 regulates synapse development and autistic-like behavior in the mouse.

S Schuster1, M Rivalan2, U Strauss3

  • 1Dendritic Development, Institute of Cell and Neurobiology, Charité Universitätsmedizin Berlin, Berlin, Germany.

Molecular Psychiatry
|April 15, 2015
PubMed
Summary

NOMA-GAP protein deficiency in mice impairs social behaviors and synapse development, characteristic of autism spectrum disorders (ASDs). Its interaction with MAGUK proteins, particularly PSD-95, is crucial for synaptic function and social behavior regulation.

More Related Videos

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism
08:44

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism

Published on: October 17, 2025

855
Strategies for Assessing Autistic-Like Behaviors in Mice
07:38

Strategies for Assessing Autistic-Like Behaviors in Mice

Published on: September 20, 2024

2.8K

Related Experiment Videos

Last Updated: Apr 15, 2026

Osmotic Avoidance in Caenorhabditis elegans: Synaptic Function of Two Genes, Orthologues of Human NRXN1 and NLGN1, as Candidates for Autism
11:20

Osmotic Avoidance in Caenorhabditis elegans: Synaptic Function of Two Genes, Orthologues of Human NRXN1 and NLGN1, as Candidates for Autism

Published on: December 11, 2009

12.3K
Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism
08:44

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism

Published on: October 17, 2025

855
Strategies for Assessing Autistic-Like Behaviors in Mice
07:38

Strategies for Assessing Autistic-Like Behaviors in Mice

Published on: September 20, 2024

2.8K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Neuropsychiatric disorders like autism spectrum disorders (ASDs) and schizophrenia involve social behavior deficits.
  • These disorders are often linked to abnormal development of dendritic spines and synapses.

Purpose of the Study:

  • To investigate the role of NOMA-GAP, a Cdc42 GTPase-activating protein, in regulating social behavior and synaptic development.
  • To elucidate the molecular mechanisms underlying NOMA-GAP's function in the context of autism-like behaviors.

Main Methods:

  • Utilized genetically engineered mice lacking NOMA-GAP.
  • Performed experiments involving Cre-mediated deletion of Cdc42.
  • Analyzed spine morphology, social behavior, protein interactions (MAGUK proteins), PSD-95 phosphorylation and localization, and AMPA receptor levels.

Main Results:

  • NOMA-GAP deficiency in mice resulted in autism-like social behaviors and impaired dendritic spine and synapse development.
  • Deleting Cdc42 alone did not restore spine morphology or social behavior in NOMA-GAP-deficient mice.
  • NOMA-GAP interacts with MAGUK proteins, modulating its activity and regulating PSD-95 phosphorylation and localization, leading to reduced surface AMPA receptors and defective synaptic transmission.

Conclusions:

  • NOMA-GAP is a key regulator of social behavior and synaptic development, potentially contributing to autism spectrum disorders.
  • NOMA-GAP's function extends beyond Cdc42 regulation, involving interactions with MAGUK proteins like PSD-95.
  • Dysregulation of the NOMA-GAP/PSD-95 pathway impacts synaptic plasticity and underlies autism-like social deficits.